Molecular and phenotypic spectrum of de novo Philadelphia positive acute leukemia.

Lim, Lay-Cheng; Heng, Kee; Vellupillai, M; Tan, Lin; Boey, B C; Lau, Lai Ching; How, Gee Fung

doi:10.3892/ijmm.4.6.665

Cited by 11 publications

(14 citation statements)

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“…236,237 Cases with de novo AML carrying BCR/ABL are most often positive for CD13, CD18 and HLA-DR. Expression of B cellrelated antigens is frequent.…”

Section: Bcr/abl Pos Amlmentioning

confidence: 99%

Antigen expression patterns reflecting genotype of acute leukemias

2002

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“…236,237 Cases with de novo AML carrying BCR/ABL are most often positive for CD13, CD18 and HLA-DR. Expression of B cellrelated antigens is frequent.…”

Section: Bcr/abl Pos Amlmentioning

confidence: 99%

Antigen expression patterns reflecting genotype of acute leukemias

2002

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“…Indeed, when results from five different studies were combined, including 170 adults and children, 94% of BCR-ABL positive ALL had a pre-B cell immunophenotype. 20,24,26,30,31 In a study by Gleissner et al 23 on 875 adult ALL patients, the prevalence of BCR-ABL positivity among CD10-expressing adult pre-B ALL was 37% whereas in the CD10-negative cohort it was only 2%. The incidence of BCR-ABL in T-cell leukemias varies among studies from 0% to 5%.…”

Section: Clinical and Immunological Correlates At Initial Diagnosismentioning

confidence: 99%

“…The incidence of BCR-ABL in T-cell leukemias varies among studies from 0% to 5%. 20,23,24,26,30,31 Coexpression of myeloid markers, as defined by CD13 or CD33 in at least 20% of blasts, is found in 27 to 29% of BCR-ABL positive adult and childhood ALL. 23,30,32 Myeloid markers are more frequently seen in BCR-ABL positive than in BCR-ABL negative ALL.…”

Section: Clinical and Immunological Correlates At Initial Diagnosismentioning

confidence: 99%

“…23,26 There was no correlation between myeloid co-expression and p190 versus p210 breakpoint, 20,30 nor was there a correlation with WBC count, blast count, hemoglobin, or hematocrit. 31 Some investigators suggest that myeloid antigen expression has an adverse impact on survival in BCR-ABL positive ALL patients while others do not. 19,30,32 Studies comparing the presenting clinical features of BCR-ABL positive versus negative ALL have also produced conflicting results.…”

Section: Clinical and Immunological Correlates At Initial Diagnosismentioning

confidence: 99%

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Clinical Applications of BCR-ABL Molecular Testing in Acute Leukemia

Nashed

Rao

Gulley

2003

The Journal of Molecular Diagnostics

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Recent advances in molecular genetics impact the health care and outcome of patients with acute lymphoblastic leukemia (ALL). BCR-ABL, a common molecular defect in adult ALLIn 1960, Nowell and Hungerford 1 reported the discovery of what came to be known as the Philadelphia chromosome (Ph 1 ) in association with chronic myelogenous leukemia (CML). Their short report entitled "Minute chromosome in human chronic granulocytic leukemias" was the first to demonstrate a leukemia-specific genetic abnormality. In the ensuing decades, the pathology of the Ph 1 has been studied and it is now known to represent an abnormally shortened (derivative) chromosome 22 resulting from translocation with chromosome 9.2 The t(9;22) is found in over 90% of CMLs, in a lesser proportion of acute lymphoblastic leukemias (ALL) or biphenotypic acute leukemias, and in rare cases of de novo acute myelogenous leukemia (AML).The break on chromosome 22q11.2 usually occurs in the major breakpoint cluster region (M-BCR), in the minor breakpoint cluster region (m-BCR), or rarely at other nearby sites. The break on chromosome 9q34 involves the ABL gene, named after Abelson murine leukemia virus where a viral version of the ABL gene was first discovered. The translocation brings the 5Ј end of the BCR gene into juxtaposition with the tyrosine kinase domain of the ABL gene to produce a hybrid gene retaining tyrosine kinase activity. 3Depending on whether the M-BCR or m-bcr breakpoint is involved in the translocation, transcription of the hybrid gene results in chimeric mRNA encoding a 210 kd BCR-ABL fusion protein or a 190 kd BCR-ABL fusion protein, respectively. The reciprocal ABL-BCR translocation also forms a chimeric gene that is capable of being transcribed, but the pathological significance of this reciprocal chimeric gene product is uncertain. Laboratory Tests for t(9;22)Conventional cytogenetics is the recommended test for detecting t(9;22) in newly diagnosed leukemia patients. Chromosome banding analysis has the advantage of high specificity and an ability to detect alternate or additional cytogenetic defects that are valuable in diagnosis and prognosis. However, cytogenetic analysis requires viable marrow cells or more than 10% blasts in the peripheral blood to reliably culture the cells and visualize metaphases. Occasionally fibrosis interferes with marrow aspiration, yielding few analyzable metaphase cells. The number of cells examined determines the sensitivity of karyotyping. A typical examination of 20 cells carries a sensitivity of one in 20, or 5%. Cryptic t(9;22) occurs in about 5% of CML cases and also in a small proportion of ALLs, resulting in false negative karyotypic interpretation in metaphase spreads of cells that actually contain the translocation at the molecular level.

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“…[35][36][37][38][39] Excellent reviews on the genes involved in AML with those common translocations providing extensive information about the molecular details and the consecutive biologic effects are presented by Appelbaum et al 40 and Friedman. 35 In addition, there are many reports about gene alterations in AML without any defined gross chromosomal abnormality such as ras-oncogene mutations, [41][42][43] p53 mutations, 44,45 pglycoprotein expression, 46 internal tandem dublication of flt3 receptor, [47][48][49] c-myc amplification, 50,51 hox overexpression 52 or nm23 expression.…”

Section: Characterization Of the Malignant Cell Clone In Acute Myeloimentioning

confidence: 99%